Introduction

Orthostatic hypotension is defined as a sudden drop in blood pressure upon standing from a sitting or supine position. Clinically, this is diagnosed by a sustained reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of 10 mmHg within three minutes of standing after being supine for five minutes or at a 60-degree angle on the tilt table. This sudden drop in blood pressure is usually secondary to failure of autonomic reflex, volume depletion, or adverse reaction to medication. Symptoms on presentation are commonly related to cerebral hypoperfusion, but patients can also be asymptomatic. There also is a high rate of morbidity and mortality related to this disease process due to frequent falls, which can lead to multiple hospital admissions. [1][2][3][4][5]

Etiology

Orthostatic hypotension can be caused by both neurogenic and non-neurogenic etiologies and can also be related to medication. Neurogenic orthostatic hypotension is characterized by autonomic instability secondary to neuropathic disease, neurodegenerative disease, or aging. Neuropathic diseases include diabetes, cholinergic receptor autoantibodies, and familial dysautonomia. Neurodegenerative diseases include Parkinson disease, multiple-system atrophy, and pure autonomic failure. Non-neurogenic orthostatic hypotension is most commonly due to volume depletion. One must also consider medication induced orthostatic hypotension particularly in the case of polypharmacy in the elderly.

Epidemiology

According to the literature, orthostatic hypotension is most prevalent in patients age 65 years or older, in part due to impaired baroreceptor sensitivity. The prevalence can be as high as 18.2% within that age range. Patients with cardiovascular disease such as aortic stenosis, pericarditis/myocarditis or arrhythmias are also at increased risk for orthostatic hypotension. It can also occur in younger and middle-age patients, who, in the absence of volume depletion, usually have a chronic autonomic failure.

Pathophysiology

There is pooling of approximately 300 mL to 800 mL of blood in the lower extremities secondary to gravitational forces immediately upon standing from a supine position. This results in decreased venous return to the heart, and as a result, there is a decrease in cardiac output as defined by the Frank Starling Curve. The human body normally compensates with an increase in sympathetic tone and a decrease in vagal tone, known as the baroreceptor reflex. This increase in sympathetic outflow raises peripheral vascular resistance, which subsequently increases venous return and cardiac output, thereby limiting the fall in blood pressure. When patients lack this compensatory mechanism, they present with symptoms of orthostatic hypotension.

History and Physical

The diagnosis of orthostatic hypotension is based entirely on a detailed history and physical exam. The physical exam must include orthostatic vital signs. All patients should be screened with orthostatic vitals, particularly in the case of the elderly. This is a simple and easy test that is often forgotten in the clinical setting.

Patients often present with generalized symptoms of lightheadedness, dizziness, or syncope and less commonly with leg buckling, headache, or chest pain. It is important to determine preceding events or precipitating events and look at the medication list. One must perform a detailed cardiovascular and neurologic exam to rule out a cardiogenic origin of the symptoms. In the elderly, it is also important to rule out neurogenic causes as well as hypovolemia secondary to diuretics, blood loss, or vomiting, and polypharmacy. Particularly in the case of syncope, it is important to rule out other common causes such as seizure and neurocardiogenic syncope (vasovagal syncope).

Evaluation

The initial evaluation of these patients requires a thorough medication reconciliation. Medications including vasodilators, diuretics, antidepressants, antipsychotics and dopaminergic drugs commonly precipitate orthostatic hypotension. Patients with no obvious cause should have a thorough cardiac evaluation beginning with an ECG as well as a laboratory evaluation to look for findings of anemia, dehydration, diabetes, alcoholism, or heart failure. One must also consider neurodegenerative disease, which is primarily diagnosed by history and physical exam.

It is essential to obtain orthostatic vital signs to make an orthostatic hypotension diagnosis. Allow the patient to rest supine while obtaining the blood pressure and heart rate. After five minutes of lying supine, the patient should be asked to stand quietly for two to five minutes, and vital signs should be taken again. If there is a 20 mmHg drop in systolic blood pressure or a 10 mmHg drop in diastolic blood pressure, one can make the diagnosis of orthostatic hypotension.[6][7][8][9]

Treatment / Management

The etiology determines the management of these patients. The treatment goal is to relieve symptoms and prevent associated morbidity. According to the literature, asymptomatic patients are left alone except for patients with Parkinson disease. These patients should be screened as they have associated impairments in their quality of life, as well as higher risk of falls. For patients with a medication-related disease, it is important to remove the offending agent and optimize the patient's medication regimen. Many patients require a multidisciplinary approach to address underlying diabetes, hypertension, Parkinson's disease and other comorbidities. Patients that are suffering from dehydration require timely volume resuscitation.

Patients with neurogenic etiology should be counseled on lower extremity stockings, abdominal binders, adequate hydration, salt intake, and fall prevention. Nonpharmacologic measures are generally sufficient. Pharmacologic treatment should be implemented after a nonpharmacologic intervention has failed to relieve symptoms. According to the literature, fludrocortisone and midodrine remain first-line medications, but many other pharmacologic therapies can be used, including pyridostigmine. Fludrocortisone is an aldosterone analogue; midodrine is an alpha-1 agonist and pyridostigmine is an acetylcholinesterase inhibitor. All of these medications work through different mechanisms in order to increase vascular tone. In a recent study, midodrine was shown to be more efficacious than pyridostigmine with regards to symptomatic relief. [10][11][12]

Pearls and Other Issues

Approximately 50% of patients with neurogenic orthostatic hypotension suffer from supine hypertension. This association is due to side effects from anti-hypertensive medications as well as the common autonomic dysfunction seen in these patients due to comorbid conditions, such as diabetes mellitus. There is currently no approved anti-hypertensive medication that selectively targets the supine position. This complicates treatment because supine hypertension in patients with autonomic failure can result in end organ damage. The treatment approach for these patients is currently being studied and might be an outlet for individualized based medicine in the future.

Enhancing Healthcare Team Outcomes

The management of orthostatic hypotension is best done with a multidisciplinary team that includes an endocrinologist, internist, primary care provider, neurologist, and nurse practitioner. The etiology determines the management of these patients. The treatment goal is to relieve symptoms and prevent associated morbidity. According to the literature, asymptomatic patients are left alone except for patients with Parkinson disease. These patients should be screened as they have associated impairments in their quality of life, as well as a higher risk of falls. For patients with a medication-related disease, it is important to remove the offending agent and optimize the patient's medication regimen. Many patients require a multidisciplinary approach to address underlying diabetes, hypertension, Parkinson's disease and other comorbidities. Patients that are suffering from dehydration require timely volume resuscitation. Overall, the prognosis of asymptomatic patients is excellent but those with symptoms tend to have a poor quality of life. [9][13](Level V)

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Orthostatic Hypotension - Questions

Take a quiz of the questions on this article.

A 72-year-old man has had several falls over the past month. He denies any dizziness, headache, tremors, gait, or visual problems preceding the falls. One year ago, he was prescribed an antidepressant (nortriptyline) for depression after his wife's death. He also takes warfarin and digoxin 0.25 mg daily for chronic atrial fibrillation. He reports that he feels well and his appetite has improved. Repeat measurements indicate that the systolic blood pressure is 155/75 mm Hg while supine and decreases to 110/70 mm Hg upon standing, without syncope or dizziness. His pulse is 78 beats per minute and irregular. His INR is 2.2. What is the next step in his management?

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A decrease in systolic blood pressure (SBP) of more than 5 mmHg and diastolic blood pressure (DBP) more than 10 mmHg

A decrease in SBP more than 10 and DBP more than 10 mmHg

A decrease in SBP more than 20 and DBP more than 20 mm Hg

A decrease in SBP more than 20 and DBP more than 10 mmHg

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A group of patients is being led in a parachute activity for sensory integration. Some of the patients have schizophrenia and are on antipsychotic medication. Which side effect of these medications would be most important during this activity?

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Provide the patient with a glass of juice as this is most likely hypoglycemia

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A patient with spinal cord injury develops severe lightheadedness and nausea after being brought to a stand at the standing table. She seems to be losing consciousness. What is the best management of this situation?

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An 85-year-old woman with a past medical history of osteopenia and hypothyroidism is evaluated in the emergency department after an episode of syncope that occurred 3 hours ago. The patient’s husband claims that she has had recurrent episodes of syncope over the past few months. According to the patient's husband, she regained consciousness within 20 seconds and experienced no confusion after the event. She has no evidence of tongue biting or incontinence. The patient states that she "passed out" when she got up from the kitchen table to get a glass of water. Her only medications are cholecalciferol 2,000 units daily and levothyroxine 75mcg daily. On physical exam, the patient is lying comfortably on the stretcher in no acute distress. Her vital signs are within normal limits. Cardiovascular and respiratory exams are benign. The patient complains of pain to palpation in the left lower quadrant of the abdomen. ECG shows normal sinus rhythm. Which of the following tests is most appropriate?

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A 72-year-old male with a past medical history of severe depression, hyperlipidemia, and obsessive compulsive disorder presents with a 3-month history of his legs "buckling" while he is standing still. He doesn't know what causes it and says that he feels fine. When he stands up he denies any dizziness, lightheadedness, or syncope. After standing for less than a minute, his legs give out and he falls. This does not occur every time he is standing. His psychiatrist is concerned with a neurologic problem and asked him to see his primary care provider. He has completed physical therapy for "leg weakness" but is still having the events. Medications include vitamin C, calcium-Vit D, clonazepam 0.5 mg nightly, topiramate 50 mg daily, and simvastatin 40 mg at bedtime. His physical exam shows his blood pressure is 133/84 mmHg, pulse 78 bpm, respiratory rate 13/min, temperature 36.4 C (97.6 F), SpO2 94% on room air, and weight 101.6 kg (224 lb). Cardiovascular and respiratory exams were unremarkable. Neurologic exam shows no cranial nerve deficits and coordination is normal. His gait is slow. The exam is otherwise unremarkable. What would be the best next step in determining the diagnosis?

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